Evidence map›Paper›PMID 29072701›Full record

ArticleCell death & disease2017

Caspase-2 deficiency enhances whole-body carbohydrate utilisation and prevents high-fat diet-induced obesity.

Claire H Wilson, Andrej Nikolic, Stephen J Kentish, Marianne Keller, George Hatzinikolas, Loretta Dorstyn, Amanda J Page, Sharad Kumar

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
6.4field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

10 citing papers in PubMed, 61 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Exploring caspase functions in mouse models.Apoptosis : an international journal on programmed cell death · 2024
    Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 5 institutions in 1 country.

Claire H WilsonCentre for Cancer Biology, University of South Australia and SA Pathology, Adelaide, South Australia, Australia.
Andrej NikolicCentre for Cancer Biology, University of South Australia and SA Pathology, Adelaide, South Australia, Australia.
Stephen J KentishAdelaide Medical School, University of Adelaide, Adelaide, South Australia, Australia.
Marianne KellerAdelaide Medical School, University of Adelaide, Adelaide, South Australia, Australia.
George HatzinikolasAdelaide Medical School, University of Adelaide, Adelaide, South Australia, Australia.
Loretta DorstynCentre for Cancer Biology, University of South Australia and SA Pathology, Adelaide, South Australia, Australia.
Amanda J PageAdelaide Medical School, University of Adelaide, Adelaide, South Australia, Australia.
Sharad KumarCentre for Cancer Biology, University of South Australia and SA Pathology, Adelaide, South Australia, Australia.
Centre for Cancer Biology · AUSouth Australian Health and Medical Research Institute · AUUniversity of Adelaide · AUSouth Australia Pathology · AUUniversity of South Australia · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Caspase-2 has been shown to be involved in metabolic homeostasis. Here, we show that caspase-2 deficiency alters basal energy metabolism by shifting the balance in fuel choice from fatty acid to carbohydrate usage. At 4 weeks of age, whole-body carbohydrate utilisation was increased in Casp2

Indexed as

AnimalsCaspase 2Diet, High-FatEnergy MetabolismGene ExpressionHumansMaleMiceObesityRatsCaspase 2

Identifiers

PMID29072701
PMCPMC5682682
OpenAlexW2766356594

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.